Increased alcohol preference and consumption, depressed mood, and impulsive aggression are thought to be linked in part through decreased central serotonergic (5-HT) activity. In agreement with this postulate, certain agents which increase central serotonergic neurotransmission (5-HT precursors, 5-HT uptake inhibitors, 5-HT receptor agonists) attenuate ethanol intake, improve memory function in intoxicated patients, and may improve memory functions in patients with Korsakoff's psychosis. Recently, a possible pattern of atypical glucose metabolism has emerged in alcohol abusing impulsive violent offenders with apparent central serotonergic dysfunction. In a group of impulsive offenders, hypoglycemia was noted during an oral glucose tolerance test. The observed hypoglycemia was possibly due to increased insulin secretion. It is possible that a relative hypoglycemic state or abnormal insulin levels may contribute to violent, aggressive behavior in violent offenders with apparently reduced central 5-HT activity; however, this hypothesis awaits substantially more scientific verification. Although appropriate animal studies have not been performed which demonstrate a cause and effect relationship between altered central serotonin activity and abnormal glucose metabolism, there is overwhelming evidence that appropriate glucose levels are maintained through a complex feedback system which involves the sympathoadrenalmedullary system through the glucose mobilizing hormone epinephrine and the endocrine pancreas via insulin and glucagon secretion.